Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk

Autores
Hinojosa Vera, Kathleen Fabiola; Hemakumar, Chandru; Bilachi, Ravindranath S.; Ramirez, Dario; Gomez Mejiba, Sandra Esther
Año de publicación
2025
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Obesity, a chronic inflammatory disease, is caused by a positive balance between energy intake and energy expenditure. Adipose tissue (AT) inflammation is the main cause of local and systemic inflammation and oxidative stress and is the link between systemic inflammation and obesity-associated metabolic abnormalities, such as dyslipidemia, hypertension, insulin resistance (IR), fatty liver disease, and dysfunction of pancreatic β-cells. AT macrophages are derived from bone marrow and blood monocytes that, upon arrival and under the pressure of the AT microenvironment, are differentiated into AT-associated macrophages (ATMs). The AT microenvironment in obesity causes the activation of transcription factors that control the expression of a number of inflammatory genes, leading to an ATM M1 phenotype or classically activated ATM. These M1 macrophages express a number of proinflammatory genes and are the main cause of AT inflammation. Herein, we reviewed recently published information on the molecular mechanisms leading to the phenotypic switch of macrophages under the pressure of obese AT. This information is needed to develop novel mechanism-based therapeutics to reduce AT inflammation and thus the metabolic risk associated with obesity.
Fil: Hinojosa Vera, Kathleen Fabiola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis. Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis; Argentina
Fil: Hemakumar, Chandru. Dayananda Sagar College of Engineering; India
Fil: Bilachi, Ravindranath S.. Manipal Academy of Higher Education; India
Fil: Ramirez, Dario. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis. Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis; Argentina
Fil: Gomez Mejiba, Sandra Esther. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis. Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis; Argentina
Materia
OBESITY
ADIPOSE TISSUE INFLAMMATION
MACROPHAGE
GENE EXPRESSION
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/290288
Acceder
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network_name_str CONICET Digital (CONICET)
spelling Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic RiskHinojosa Vera, Kathleen FabiolaHemakumar, ChandruBilachi, Ravindranath S.Ramirez, DarioGomez Mejiba, Sandra EstherOBESITYADIPOSE TISSUE INFLAMMATIONMACROPHAGEGENE EXPRESSIONhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Obesity, a chronic inflammatory disease, is caused by a positive balance between energy intake and energy expenditure. Adipose tissue (AT) inflammation is the main cause of local and systemic inflammation and oxidative stress and is the link between systemic inflammation and obesity-associated metabolic abnormalities, such as dyslipidemia, hypertension, insulin resistance (IR), fatty liver disease, and dysfunction of pancreatic β-cells. AT macrophages are derived from bone marrow and blood monocytes that, upon arrival and under the pressure of the AT microenvironment, are differentiated into AT-associated macrophages (ATMs). The AT microenvironment in obesity causes the activation of transcription factors that control the expression of a number of inflammatory genes, leading to an ATM M1 phenotype or classically activated ATM. These M1 macrophages express a number of proinflammatory genes and are the main cause of AT inflammation. Herein, we reviewed recently published information on the molecular mechanisms leading to the phenotypic switch of macrophages under the pressure of obese AT. This information is needed to develop novel mechanism-based therapeutics to reduce AT inflammation and thus the metabolic risk associated with obesity.Fil: Hinojosa Vera, Kathleen Fabiola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis. Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis; ArgentinaFil: Hemakumar, Chandru. Dayananda Sagar College of Engineering; IndiaFil: Bilachi, Ravindranath S.. Manipal Academy of Higher Education; IndiaFil: Ramirez, Dario. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis. Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis; ArgentinaFil: Gomez Mejiba, Sandra Esther. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis. Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis; ArgentinaMDPI2025-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/290288Hinojosa Vera, Kathleen Fabiola; Hemakumar, Chandru; Bilachi, Ravindranath S.; Ramirez, Dario; Gomez Mejiba, Sandra Esther; Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk; MDPI; Preprints; 5-2025; 1-242310-287XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.preprints.org/manuscript/202505.1869/v1info:eu-repo/semantics/altIdentifier/doi/10.20944/preprints202505.1869.v1info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2026-08-25T14:37:26Zoai:ri.conicet.gov.ar:11336/290288instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982026-08-25 14:37:26.366CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk
title Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk
spellingShingle Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk
Hinojosa Vera, Kathleen Fabiola
OBESITY
ADIPOSE TISSUE INFLAMMATION
MACROPHAGE
GENE EXPRESSION
title_short Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk
title_full Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk
title_fullStr Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk
title_full_unstemmed Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk
title_sort Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk
dc.creator.none.fl_str_mv Hinojosa Vera, Kathleen Fabiola
Hemakumar, Chandru
Bilachi, Ravindranath S.
Ramirez, Dario
Gomez Mejiba, Sandra Esther
author Hinojosa Vera, Kathleen Fabiola
author_facet Hinojosa Vera, Kathleen Fabiola
Hemakumar, Chandru
Bilachi, Ravindranath S.
Ramirez, Dario
Gomez Mejiba, Sandra Esther
author_role author
author2 Hemakumar, Chandru
Bilachi, Ravindranath S.
Ramirez, Dario
Gomez Mejiba, Sandra Esther
author2_role author
author
author
author
dc.subject.none.fl_str_mv OBESITY
ADIPOSE TISSUE INFLAMMATION
MACROPHAGE
GENE EXPRESSION
topic OBESITY
ADIPOSE TISSUE INFLAMMATION
MACROPHAGE
GENE EXPRESSION
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Obesity, a chronic inflammatory disease, is caused by a positive balance between energy intake and energy expenditure. Adipose tissue (AT) inflammation is the main cause of local and systemic inflammation and oxidative stress and is the link between systemic inflammation and obesity-associated metabolic abnormalities, such as dyslipidemia, hypertension, insulin resistance (IR), fatty liver disease, and dysfunction of pancreatic β-cells. AT macrophages are derived from bone marrow and blood monocytes that, upon arrival and under the pressure of the AT microenvironment, are differentiated into AT-associated macrophages (ATMs). The AT microenvironment in obesity causes the activation of transcription factors that control the expression of a number of inflammatory genes, leading to an ATM M1 phenotype or classically activated ATM. These M1 macrophages express a number of proinflammatory genes and are the main cause of AT inflammation. Herein, we reviewed recently published information on the molecular mechanisms leading to the phenotypic switch of macrophages under the pressure of obese AT. This information is needed to develop novel mechanism-based therapeutics to reduce AT inflammation and thus the metabolic risk associated with obesity.
Fil: Hinojosa Vera, Kathleen Fabiola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis. Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis; Argentina
Fil: Hemakumar, Chandru. Dayananda Sagar College of Engineering; India
Fil: Bilachi, Ravindranath S.. Manipal Academy of Higher Education; India
Fil: Ramirez, Dario. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis. Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis; Argentina
Fil: Gomez Mejiba, Sandra Esther. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis. Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto Multidisciplinario de Investigaciones Biológicas de San Luis; Argentina
description Obesity, a chronic inflammatory disease, is caused by a positive balance between energy intake and energy expenditure. Adipose tissue (AT) inflammation is the main cause of local and systemic inflammation and oxidative stress and is the link between systemic inflammation and obesity-associated metabolic abnormalities, such as dyslipidemia, hypertension, insulin resistance (IR), fatty liver disease, and dysfunction of pancreatic β-cells. AT macrophages are derived from bone marrow and blood monocytes that, upon arrival and under the pressure of the AT microenvironment, are differentiated into AT-associated macrophages (ATMs). The AT microenvironment in obesity causes the activation of transcription factors that control the expression of a number of inflammatory genes, leading to an ATM M1 phenotype or classically activated ATM. These M1 macrophages express a number of proinflammatory genes and are the main cause of AT inflammation. Herein, we reviewed recently published information on the molecular mechanisms leading to the phenotypic switch of macrophages under the pressure of obese AT. This information is needed to develop novel mechanism-based therapeutics to reduce AT inflammation and thus the metabolic risk associated with obesity.
publishDate 2025
dc.date.none.fl_str_mv 2025-05
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/290288
Hinojosa Vera, Kathleen Fabiola; Hemakumar, Chandru; Bilachi, Ravindranath S.; Ramirez, Dario; Gomez Mejiba, Sandra Esther; Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk; MDPI; Preprints; 5-2025; 1-24
2310-287X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/290288
identifier_str_mv Hinojosa Vera, Kathleen Fabiola; Hemakumar, Chandru; Bilachi, Ravindranath S.; Ramirez, Dario; Gomez Mejiba, Sandra Esther; Phenotypic Switch of Adipose Tissue Macrophages as a Target to Reduce Obesity-Associated Metabolic Risk; MDPI; Preprints; 5-2025; 1-24
2310-287X
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.preprints.org/manuscript/202505.1869/v1
info:eu-repo/semantics/altIdentifier/doi/10.20944/preprints202505.1869.v1
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.265058

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